Atrial fibrillation is the rapid and asynchronous contraction of individual muscle fibers within the atria of the heart. One result of this fibrillation within the atrium is functional loss of the augmented pumping capability of the heart. Normally the atria operate in very low pressure states such that loss of atrial contraction will not lead to cessation of blood flow and death. During atrial fibrillation the blood continues to flow passively through the atria into the ventricles with only a 10-15% diminution of blood flow. Depending on total cardiac reserves and patient status, this diminution of cardiac output may or may not be symptomatic to the patient.
A second effect of atrial fibrillation is a rapid ventricular response. The classic clinical description is a rapid irregularly irregular heart rate. This irregular irregularity is caused by incomplete or partial conduction of the atrial fibrillation currents arriving at the AV node. The atrial fibrillation rates are extremely high and are usually not conducted on a one-to-one basis. Instead, as the AV node receives one signal and passes it on, the AV node enters a short refractory period during which it will not respond to any other subsequent atrial fibrillation. When the refractory period ends the AV node is again sensitive to atrial fibrillation currents. When the next fibrillation current arrives, the AV node responds by triggering the next ventricular contraction. Since there are far more atrial fibrillation currents the overall ventricular rate increases but is irregularly irregular due to the refractory periods of the conduction system.
This rise in the ventricular response rate also affects hemodynamic stability by decreasing diastolic filling times. The contraction time period for the ventricles during systole is generally the same length, regardless of pulse rate. Therefore, in order to increase pulse rate, then the time between successive systolic events, i.e., the diastolic period, must shorten. Since the only time available to the heart to refill the ventricles is during diastole, a decrease in this time period leads to a decrease in refilling the ventricles. The heart has less blood for the next contraction causing additional diminution of cardiac output.
A further complication secondary to this irregular rate is timing of the atrial defibrillation countershock. Studies have shown that although atrial defibrillation is a reliable treatment modality, in a few percent of the cases the atrial defibrillating countershock will cause fibrillation in the ventricles. The irregularly irregular ventricular rate forces a randomly timed countershock. If a defibrillation countershock to the atria inadvertently occurs during the T wave of the ventricular cycle, ventricular fibrillation may be precipitated. Ventricular fibrillation is life threatening and requires further immediate countershock therapy to the ventricles and therefore is best avoided.
An additional secondary effect of atrial fibrillation and the passive blood flow through the atrial chambers is formation of mural thrombi. Formation of these blood clots is generally avoided if atrial fibrillation is treated successfully within a time period ranging from minutes to several hours after onset. Once formed, these thrombi become sources of embolization to both the pulmonary as well as the systemic circulations. Embolization to the pulmonary vasculature leads to decreased oxygenation and carbon dioxide exchange within the lungs. Since all of the output of the right side of the heart circulates to the lungs, all clots embolized from the right atrium will lodge in the lungs. Death can ensue if the degree of embolization is severe enough. Embolization to the systemic vascular system leads to strokes if the embolus travels to the brain. Other organ injury occurs depending upon where the embolus stopped.
Ideally, the treatment of atrial fibrillation is performed in such a manner that there is reasonably prompt conversion of the atrial fibrillation back into an organized atrial contraction with subsequent capture of the ventricles. There are a number of atrial cardioverter/defibrillator systems which are known. These systems generally comprise either isolated atrial systems or are in combination with ventricular defibrillation systems. A number of electrode configurations are also disclosed in conjunction with the various systems.